Nasal sinus disease is one of the most common medical conditions in the US, affecting an estimated 13% of adults, or some 30 million people and responsible for 5.8 billion in healthcare costs annually (National Health Interview Survey 2009, CDC). Nasal obstruction and smell loss are two of the major symptoms of the disease; however, the field currently lacks a clear, objective understanding to the mechanisms causing these symptoms, which thwarts effective treatment. For example, patients' complaints of nasal obstruction correlate poorly or inconsistently with objective measurements of actual physical obstruction. Olfactory loss has been widely believed to be induced in part by airflow blockage; however, no tool has been able to quantify or predict such conductive mechanism. Without validated clinically tools, current evaluation and treatment on these symptoms rely primarily on the patient's subjective feedback and the doctor's personal training and experience. We propose to objectively evaluate the conductive components underling nasal obstructive symptoms, based on two hypotheses (a) that perception of nasal obstruction (lack of patency) may be caused not by obstruction per se but by lack of nasal cooling, and that such perception can be worsened by inadequate trigeminal feedback in the nasal airways, and (b) that insufficient air/odorant flow specifically to the olfactory region causes conductive olfactory losses. To test these hypotheses and pursue a clinical tool, we will study several types of patients with chronic complaints of nasal obstruction or smell loss: turbinate hypertrophy, septal deviation, idiopathic nasal obstruction, and nasal polyps. In Aim 1, we will use individualized CFD models based on easily obtained office CT scans to capture the insufficient mucosal cooling due to airway abnormalities and determine if this alone or in combination with conventional rhinometric measurements predicts patient complaints of nasal obstruction at several time points post treatment/surgery. A nasal dilator and decongestant will be used to temporarily perturb patients' nasal airways, to test whether our approach can predict perceptual symptom changes. In Aim 2, we will broadly assess the trigeminal cool sensitivity of patients with the symptom of nasal obstruction, and determine whether abnormal trigeminal cool sensitivity (including the TRPM8 pathway) contributes to symptoms. TRPM8 is a major component of the cool afferent pathway that is also activated chemically, which offers a unique dual investigatory tool and potentially broadens our understanding of chemosensory functions in nasal inflammatory disease. Variables from both aims will be combined to form the final evaluation tool for nasal obstruction symptom. In Aim 3, we will specifically target nasal polyp patients with olfactory losses, track their treatment/surgery progress, and determine if the CFD-predicted airflow and odorant sorption rate to the olfactory region correlate with olfactory losses and recovery. The outcomes from this research may validate how to combine one or several measurements into an effective clinical tool to evaluate the causal factors leading to a patient's conductive symptoms, to potentially identify the site that most affects the symptom, and to assist patients and clinicians n planning effective, well-informed, personalized treatment/surgery strategies, potentially saving millions of healthcare dollars annually while improving patient satisfaction.